Loss of the function or number of pancreatic β-cells in a subject contributes to the pathogenesis of several diseases, including type 1 diabetes (diabetes mellitus), type 2 diabetes, and Wolfram syndrome. In type 1 diabetes, the patient has high blood glucose levels because of insulin deficiency. Generally speaking, absolute deficiency of insulin occurs in patients with type 1 diabetes, whereas relative deficiency of insulin occurs in patients with type 2 diabetes. Increasing evidence indicates that reduced functional pancreatic β-cell mass is a common feature of both type 1 and type 2 diabetes, as well as genetic forms of diabetes such as Wolfram syndrome (Pipeleers et al., Novartis Found Symp. 292:19-24, 2008). During the progression of type 1 or type 2 diabetes, pancreatic β-cell function and mass gradually decline, eventually leading to insulin deficiency and hyperglycemia. Recent findings indicate that “stressed” pancreatic β-cells are susceptible to dysfunction and death (Oslowski et al., Curr. Opin. Endocrinol. Diabetes Obes. 17:107-112, 2010; Oslowski et al., Curr. Opin. Cell Biol. 23:207-215, 2011; Fonseca et al., Trends Endocrinol. Metab. 22:266-274, 2011). Diagnostic markers that aid in predicting the susceptibility of a subject to develop pancreatic β-cell dysfunction and death will be helpful for treating or delaying the progression of pancreatic β-cell disorders (e.g., type 1 or type 2 diabetes) in subjects.